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1.
Rev. cientif. cienc. med ; 20(2): 26-32, 2017. ilus
Artigo em Espanhol | LILACS | ID: biblio-900268

RESUMO

INTRODUCCIÓN: El accidente cerebrovascular (ACV) es una lesión neurológica aguda con dos subtipos clásicos (isquémico y hemorrágico); siendo un importante problema de salud púbica en Chile. Existen patologías que imitan su presentación, sin embargo, una historia clínica y examen físico orientado permiten discriminar en un alto número de casos entre estas patologías evitando la derivación a especialista y solicitud de exámenes imagenológicos, disminuyendo así, los costos derivados en un gran número de pacientes. MATERIAL Y MÉTODO: Estudio transversal a partir de las fichas clínicas de pacientes ingresados con sospecha de ACV durante febrero y marzo del 2016 en Hospital Clínico Herminda Martín de Chillán para su confirmación diagnóstica por el Servicio de Neurología. RESULTADOS: Se obtuvieron 304 fichas clínicas con sospecha de ACV de las cuales un 26,9% no correspondieron a ACV. De estos, 45,9% eran patologías de especialidades no neurológicas siendo las más frecuentes las derivadas de Medicina Interna. DISCUSIÓN: El ACV es una entidad neurológica clásicamente descrita en base a la ubicación de la lesión vascular. Pese a que su presentación semiológica es conocida, existen muchas patologías que son clínicamente similares, o bien, las características singulares de los pacientes hacen que el patrón clínico sea confuso. Este fenómeno se refleja en una tasa de falsos ACV relativamente similar entre diferentes centros de salud. La tasa de error en diagnóstico de ACV en el estudio es de 26,9%, similar a otras experiencias. Pareciera ser que existe un número basal de falsos ACV, cuyo margen de error clínico, resulta difícil reducir aún con buenas escalas y protocolos estandarizados de atención.


INTRODUCTION: Stroke is an acute neurological lesion with two classic subtypes (ischemic and hemorrhagic), being an important public health problem in Chile. There are pathologies that mimic its presentation, however, a clinical history and oriented physical examination allow to discriminate in a high number of cases between these pathologies avoiding the referral to specialist and request of imaging examinations, thus reducing, the costs derived in a large number of patients. MATERIAL AND METHOD: Cross-sectional study from the clinical records of patients admitted with suspected stroke during February and March of 2016 at Herminda Martin Clinic Hospital from Chile for diagnostic confirmation by the Neurology Service. RESULTS: A total of 304 clinical files were obtained with suspected stroke, of which 26,9% did not correspond to stroke. Of these, 45,9% were pathologies of non-neurological specialties, the most frequent being those derived from internal medicine. DISCUSSION: Stroke is a neurological entity classically described based on the location of the vascular lesion. Although its semiologic presentation is known, there are many pathologies that are clinically similar, or the unique characteristics of the patients make the clinical pattern confusing. This phenomenon is reflected in a relatively similar false stroke rate among different health centers. The error rate in diagnosis of stroke of this study is 26,9%, similar to other experiences. It appears that there is a basal number of false stroke, whose clinical margin of error is difficult to reduce even with good scales and standardized care protocols.


Assuntos
Humanos , Acidente Vascular Cerebral , Neuropsiquiatria , Doenças do Sistema Nervoso
2.
Rheumatology (Oxford) ; 47(8): 1144-50, 2008 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-18522961

RESUMO

OBJECTIVE: We have recently reported that natural antibodies against phosphorylcholine (anti-PC) have atheroprotective properties. Here we compare anti-PC with other autoantibodies in SLE patients with and without cardiovascular disease (CVD). METHODS: Twenty-six women (52 +/- 8.2 yrs) with SLE and a history of CVD (SLE cases) were compared with 26 age-matched women with SLE without CVD (SLE controls) and 26 age-matched population-based control women (controls). PC was conjugated with BSA (PC-BSA) or keyhole-limpet haemocyanin (PC-KLH). Anti-PC and antibodies against phosphatidylserine (anti-PS) and BSA (anti-BSA) were studied by ELISA. Anti-PC-IgG were extracted from intravenous immunoglobulin (IVIG). Activation of endothelial cells by platelet-activating factor (PAF) was studied with FACScan. RESULTS: IgG anti-PC-BSA and anti-PC-KLH were decreased among SLE-cases and SLE-controls as compared with controls (P < 0.005 and P < 0.05), respectively. SLE cases were more prevalent in the lowest 25th percentile of anti-PC-IgM (and IgG) as compared with controls (P < 0.05) but anti-PC-IgM levels did not differ significantly between groups. Among SLE controls, anti-PC-BSA were associated negatively with organ damage (SLICC) and disease activity (SLEDAI) (P < 0.05). Among SLE cases, anti-PC-BSA and anti-PC-KLH were associated negatively with SLICC (P = 0.021; P = 0.010) and anti-PC-BSA was negatively associated with SLEDAI (P < 0.039). Anti-PS-IgG and anti-BSA-IgG were raised among SLE cases as compared with other groups (P < 0.05) and did not cross-react with anti-PC. Anti-PC-IgG could be extracted from IVIG and inhibited PAF-induced expression of adhesion molecules. CONCLUSION: Low levels of anti-PC could be of importance in SLE. Anti-BSA and anti-PS and low levels of anti-PC could contribute to development of CVD in SLE.


Assuntos
Autoanticorpos/sangue , Lúpus Eritematoso Sistêmico/imunologia , Fosforilcolina/imunologia , Adulto , Ligação Competitiva , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/imunologia , Reações Cruzadas , Endotélio Vascular/imunologia , Feminino , Hemocianinas/imunologia , Humanos , Imunoglobulina G/sangue , Molécula 1 de Adesão Intercelular/metabolismo , Lúpus Eritematoso Sistêmico/complicações , Pessoa de Meia-Idade , Fosforilcolina/análogos & derivados , Fator de Ativação de Plaquetas/imunologia , Soroalbumina Bovina/imunologia , Índice de Gravidade de Doença , Molécula 1 de Adesão de Célula Vascular/metabolismo
3.
Br J Haematol ; 141(4): 445-53, 2008 May.
Artigo em Inglês | MEDLINE | ID: mdl-18341636

RESUMO

TP53 is mutated in 10-20% of cases of chronic lymphocytic leukaemia (CLL) and 3-8% of cases of acute myeloid leukaemia (AML). Recently, two classes of compounds that restore the function of p53 in tumours have been described. PRIMA-1 (p53-dependent reactivation and induction of massive apoptosis) restores the wild-type conformation of mutant TP53, whereas RITA (reactivation of p53 and induction of tumour cell apoptosis) increases intracellular levels of p53. We evaluated the effects of RITA alone and in combination with PRIMA-1 or conventional cytostatics on leukaemic cells isolated from AML and CLL patients. AML samples with -17, which are more resistant to daunorubicin and cytarabine compared with samples without -17, were effectively killed by PRIMA-1. RITA, which stabilizes the function of wild-type p53, induced apoptosis in AML cells. In contrast to that seen with PRIMA-1, AML patient samples without -17 were significantly more sensitive to RITA. Similarly, RITA exerted dose-dependent apoptosis and cytotoxicity in CLL cells, which was significantly more pronounced in samples without hemizygous TP53 deletion. Notably, a synergistic effect was observed in all CLL samples with RITA and fludarabine in combination. In both AML and CLL cells exposure to RITA resulted in induction of intracellular p53. We conclude that small molecules targeting p53 might be of clinical importance in the future for treating drug-resistant leukaemia.


Assuntos
Genes p53/genética , Leucemia Linfocítica Crônica de Células B/genética , Leucemia Mieloide Aguda/genética , Mutação , Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Ciclo Celular/efeitos dos fármacos , Morte Celular/efeitos dos fármacos , Aberrações Cromossômicas , Citarabina/farmacologia , Daunorrubicina/farmacologia , Relação Dose-Resposta a Droga , Sinergismo Farmacológico , Furanos/farmacologia , Humanos , Leucemia Linfocítica Crônica de Células B/metabolismo , Leucemia Linfocítica Crônica de Células B/patologia , Leucemia Mieloide Aguda/metabolismo , Leucemia Mieloide Aguda/patologia , Proteínas de Membrana/farmacologia , Proteínas do Tecido Nervoso/farmacologia , Células Tumorais Cultivadas , Proteína Supressora de Tumor p53/metabolismo , Vidarabina/análogos & derivados , Vidarabina/farmacologia
4.
J Neurosci Res ; 82(3): 432-41, 2005 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-16184608

RESUMO

The mechanisms associated with cell death have been an important focus for neurobiology research. In the present study, the methodology of flow cytometry was used to optimize quantification of the toxic effects of tumor necrosis factor-alpha (TNF-alpha), trans-4-hydroxy-2-nonenal (4-HNE), and aged amyloid-beta (Abeta1-42) on rat primary cortical neurons. The fluorescent dyes annexin V-FITC and propidium iodide (PI) were used to identify populations of viable, early apoptotic, necrotic and late apoptotic cells by flow cytometry. Prior to exposure, the primary cultures showed 83% cell viability. Flow cytometry following labeling of cells with a specific neuronal marker, TUJ-1, revealed 82% pure neuronal populations, whereas approximately 7% were astrocytic as shown by glial fibrillary acidic protein positivity. Exposure of primary cultures to TNF-alpha, 4-HNE, and aged Abeta1-42 gave an increased number of early apoptotic cells. We show that flow cytometry is a suitable method for quantifying effects of different stressors on neurons in primary cultures. This technique could be useful for screening and testing of pharmacological compounds relevant to neurodegenerative disorders.


Assuntos
Córtex Cerebral/metabolismo , Citometria de Fluxo/métodos , Doenças Neurodegenerativas/metabolismo , Neurônios/metabolismo , Estresse Oxidativo/fisiologia , Aldeídos/farmacologia , Peptídeos beta-Amiloides/farmacologia , Animais , Apoptose/efeitos dos fármacos , Apoptose/fisiologia , Biomarcadores/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/fisiologia , Células Cultivadas , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/fisiopatologia , Modelos Animais de Doenças , Necrose/induzido quimicamente , Necrose/metabolismo , Necrose/fisiopatologia , Doenças Neurodegenerativas/fisiopatologia , Neuroglia/efeitos dos fármacos , Neuroglia/metabolismo , Neurônios/efeitos dos fármacos , Neurotoxinas/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Fragmentos de Peptídeos/farmacologia , Ratos , Ratos Sprague-Dawley , Tubulina (Proteína)/metabolismo , Fator de Necrose Tumoral alfa/farmacologia
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